The objectives of this proposal are to determine the neural substrates in the rodent hindbrain through which gustatory stimuli guide ingestive behavior. The regulation of ingestive behavior is exceedingly complex, involving widespread regions of the central nervous system, but the basic regulatory function of taste to determine palatable from unpalatable stimuli is complete in the caudal brainstem. Anatomical studies suggest that polysynaptic pathways in the reticular formation serve as an interface between the gustatory region of the nucleus of the solitary tract and the oromotor nuclei that produce the consummatory responses of ingestion and rejection. Delineating this local circuitry is prerequisite to understanding how descending forebrain pathways further influence consummatory function. Specific subdivisions of the reticular formation including the lateral parvocellular and intermediate zones are hypothesized to mediate specific components of sensorimotor coordination. The proposed experiments combine several techniques to further understand the connectivity, neurochemistry and function of these reticular regions by (1) using double-labeling immunohistochemistry for identification of neurotransmitter phenotypes with concomitant increases in the expression of the immediate early gene c-fos produced by gustatory stimulation, (2) assessing the connectivity and neurochemical phenotype of interneurons with projections to specific pools of lingual and masticatory motorneurons assayed with double labeling techniques that use the transynaptic properties of two genetically altered strains of pseudorabies virus, (3) determining the effects of reversible inactivation of small regions of the reticular formation following microinfusions of either lidocaine or antagonists to suspected neurotransmitters in the circuitry on ingestion and rejection elicited with intraoral stimulation and measured electromyographically from a subset of lingual, masticatory and pharyngeal muscles. Chronic diseases such as obesity, hypertension, and anorexia nervosa all involve ingestive dysfunction. Understanding the neurological basis of the fundamental biological decision to ingest or reject food will contribute to the eventual solution of these chronic debilitating disorders.